Abstract
BackgroundCalumenin (CALU) has been reported to be associated with invasiveness and metastasis in some malignancies. However, in glioma, the role of CALU remains unclear.MethodsClinical and transcriptome data of 998 glioma patients, including 301 from CGGA and 697 from TCGA dataset, were included. R language was used to perform statistical analyses.ResultsCALU expression was significantly upregulated in more malignant gliomas, including higher grade, IDH wildtype, mesenchymal, and classical subtype. Gene Ontology analysis revealed that CALU-correlated genes were mainly enriched in cell/biological adhesion, response to wounding, and extracellular matrix/structure organization, all of which were strongly correlated with the epithelial-mesenchymal transition (EMT) phenotype. GSEA further validated the profound involvement of CALU in EMT. Subsequent GSVA suggested that CALU was particularly correlated with three EMT signaling pathways, including TGFβ, PI3K/AKT, and hypoxia pathway. Furthermore, CALU played synergistically with EMT key markers, including N-cadherin, vimentin, snail, slug, and TWIST1. Survival and Cox regression analysis showed that higher CALU predicted worse survival, and the prognostic value was independent of WHO grade and age.ConclusionsCALU was correlated with more malignant phenotypes in glioma. Moreover, CALU seemed to serve as a pro-EMT molecular target and could contribute to predict prognosis independently in glioma.
Highlights
In central nervous system, glioma is the most prevalent and fatal primary cancer in adults [1]
These results concordantly indicated that CALU might contribute to malignant progression of glioma, which were in line with the results from a previous GBM study [22]
Gene Ontology analysis (GO) analysis was performed to elucidate the biological function of CALU in glioma and it revealed that CALU showed high association with multiple epithelial-mesenchymal transition (EMT)-related biological processes, including cell adhesion, biological adhesion, extracellular matrix/structure organization, collagen fibril organization, and collagen biosynthetic process
Summary
Glioma is the most prevalent and fatal primary cancer in adults [1]. For patients who suffered from higher grade glioma (WHO grade IV, glioblastoma, GBM), which is the most malignant and lethal type, the median survival remains less than 15 months [2,3]. There is a growing recognition that epithelial-mesenchymal transition (EMT) plays a key role in mediating tumorigenesis, stemness, invasiveness, resistance to radiochemotherapy, and early recurrence in glioma [4,5,6,7]. In most types of cancer, a higher level of CALU in lesions indicated a more malignant phenotype and a shorter survival for patients. We analyzed clinical and transcriptome data of 998 patients, aiming at exploring the role of CALU in gliomas. Gaussian test was performed before data analysis that required Gaussian distribution.
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